The present invention relates generally to the field of electrosurgery, and more particularly to surgical devices and methods which employ high frequency electrical energy to treat tissue in regions of the heart, particularly the leaflets on various heart valves. The present invention is particularly suited for removing calcified deposits and fibroid tissue from valve leaflets and the treatment of aortic stenosis.
Recently there has been growing interest in the repair of diseased native heart valves as an alternative to prosthetic valve replacement. With operative mortality between about 5% and 12% (higher among the elderly), the risk associated with valve replacement is significant. In addition, a patient receiving a replacement valve typically must take anticoagulation drugs for the rest of his or her life. Not all patients are capable of doing this. Moreover, some patients have an aortic root that is not large enough to easily accommodate conventional replacement valves. Thus, there are a significant number of patients for whom valve replacement is either impossible, impractical, or undesirable. Preservation of native tissue by valve repair is a preferable modality to valve replacement due to imperfections in most valve substitutes, and the potential complications resulting from these prostheses, including thromboembolic events, bleeding associated with anticoagulation, bacterial endocarditis, valve thrombosis, valvular mechanical complications, and degeneration of tissue valves.
Degradation of heart valve performance can be traced in part to deposits of plaque and calcified material on the valve. The leaflets of the valve are slightly thickened and coarse calcified particles and atheromatous deposits fill the belly of the valve cusps. For aortic stenosis, the buildup of calcified nodules occurs on the upper or superior surface of the aortic valve leaflets. These nodules decrease the flexibility of the leaflets, thereby limiting their mobility and capacity to fully open to permit adequate blood flow. Large calcifications in the sinus of the cusps also hinders the mobility of the valve. In addition, heavily calcified valve annulus presents a risk to the surgeon performing prosthetic aortic valve placement, as needles have difficulty in piercing calcified plaque and could fracture the plaque. Histological findings present fibrosis and calcification of the valvular annulus and the proximal parts of the cusps, with calcifications often extending to the commissures (the locations where the valve leaflets meet).
Unfortunately, current methods of repairing thickened and/or calcified valves through the removal of these deposits have significant disadvantages. Currently, high speed debriders, in combination with conventional mechanical instruments (e.g., forceps, rongeurs, scalpels), are used to removal calcified deposits. These mechanical methods are unsatisfactory as they produce tissue fragments which must be carefully and completely removed from the interior of the heart. Packs must be placed in the left ventricle to prevent the passage of calcified fragments into the heart. The area of treatment using conventional methods is also limited as general valve repair is usually not attempted if calcifications extends to the ventricular aspects of the cusps, if gross distortion of the normal architecture of the cusps is present, or if extensive commissural fusion is demonstrated.
Balloon-valvuloplasty, where a balloon catheter is inflated in the aortic valve to compress and fracture the calcified nodules in an attempt to increase leaflet mobility, has generally not been very effective in treating this type of stenosis. This is mainly because the calcified commissural parts of the cusps make it extremely difficult (if not impossible) to enlarge the valve area.
Lasers and ultrasound techniques for removing calcium deposits, though initially promising, cause deep tissue damage which permanently changes the characteristics of the valve leaflets. For example, when lasers are used for total leaflet debridement, they usually result in substantial tissue charring which causes thermal degradation of the connective tissue component of aortic valve leaflets. Damage to the connective tissue creates problems similar to those created by the calcium deposits (i.e. reduced mobility, flow regurgitation, etc.). Additionally, lasers are cumbersome to employ and have thus far been limited to in vitro debridement of aortic valves. Ultrasonic debridement of calcified deposits has similar drawbacks. Ultrasonic energy typically causes an intense healing response in the thin, flexible debrided leaflet that develops leaflet thickening and shrinkage. Such healing changes the flexural characteristics of the leaflet, creating high rates of post-procedure aortic insufficiency and regurgitation.
Accordingly, improved devices and methods are needed to decalcify heart valve leaflets while minimizing damage to the valves and substantially preserving the elastic fiber layer of the valve leaflets. The preservation of the elastic fiber layer of valve leaflets will play an important role in preventing later stenosis or regurgitation. Such an improved system would significantly enhance the options available to surgeons performing valve repair and replacement procedures.